Dysfunction In Posttraumatic Stress Disorder Research Articles

Trauma exposure acutely alters neural function during Pavlovian fear conditioning

Posttraumatic stress disorder (PTSD) is associated with dysfunction of the neural circuitry that supports fear learning and memory processes. However, much of what is known about neural dysfunction in PTSD is based on research in chronic PTSD populations. Less is known about neural function that supports fear learning acutely following trauma exposure. Determining the acute effects of trauma exposure on brain function would provide new insight into the neural processes that mediate the cognitive-affective dysfunction associated with PTSD. Therefore, the present study investigated neural activity that supports fear learning and memory processes in recently Trauma-Exposed (TE) and Non-Trauma-Exposed (NTE) participants. Participants completed a Pavlovian fear conditioning procedure during functional magnetic resonance imaging (fMRI). During fMRI, participants’ threat expectancy was continuously monitored. NTE participants showed greater threat expectancy during warning than safety cues, while no difference was observed in the TE group. This finding suggests TE participants overgeneralized the fear association to the safety cue. Further, only the TE group showed a negative relationship between fMRI signal responses within dorsomedial prefrontal cortex (PFC) and threat expectancy during safety cues. These results suggest the dorsomedial PFC mediates overgeneralization of learned fear as an acute result of trauma exposure. Finally, neural activity within the PFC and inferior parietal lobule showed a negative relationship with PTSD symptom severity assessed three months posttrauma. Thus, neural activity measured acutely following trauma exposure predicted future PTSD symptom severity. The present findings elucidate the acute effects of trauma exposure on cognitive-affective function and provide new insight into the neural mechanisms of PTSD.

Brain circuit dysfunction in post-traumatic stress disorder: from mouse to man.

Post-traumatic stress disorder (PTSD) is a prevalent, debilitating and sometimes deadly consequence of exposure to severe psychological trauma. Although effective treatments exist for some individuals, they are limited. New approaches to intervention, treatment and prevention are therefore much needed. In the past few years, the field has rapidly developed a greater understanding of the dysfunctional brain circuits underlying PTSD, a shift in understanding that has been made possible by technological revolutions that have allowed the observation and perturbation of the macrocircuits and microcircuits thought to underlie PTSD-related symptoms. These advances have allowed us to gain a more translational knowledge of PTSD, have provided further insights into the mechanisms of risk and resilience and offer promising avenues for therapeutic discovery.

Cerebellar and Prefrontal Cortical Alterations in PTSD: Structural and Functional Evidence

Background Neuroimaging studies have revealed that disturbances in network organization of key brain regions may underlie cognitive and emotional dysfunction in posttraumatic stress disorder (PTSD). Examining both brain structure and function in the same population may further our understanding of network alterations in PTSD. Methods We used tensor-based morphometry and intrinsic connectivity distribution to identify regions of altered volume and functional connectivity in unmedicated individuals with PTSD (n = 21) and healthy comparison participants (n = 18). These regions were then used as seeds for follow-up anatomical covariance and functional connectivity analyses. Results Smaller volume in the cerebellum and weaker structural covariance between the cerebellum seed and the middle temporal gyrus were observed in the PTSD group. Individuals with PTSD also exhibited lower whole-brain connectivity in the cerebellum, dorsolateral prefrontal cortex (dlPFC) and medial prefrontal cortex. Functional connectivity in the cerebellum and grey matter volume in the dlPFC were negatively correlated with PTSD severity as measured by the DSM-5 PTSD Checklist (PCL-5; r = −.0.77, r = − 0.79). Finally, seed connectivity revealed weaker connectivity within nodes of the central executive network (right and left dlPFC), and between nodes of the default mode network (medial prefrontal cortex and cerebellum) and the supramarginal gyrus, in the PTSD group. Conclusion We demonstrate structural and functional alterations in PTSD converging on the PFC and cerebellum. Whilst PFC alterations are relatively well established in PTSD, the cerebellum has not generally been considered a key region in PTSD. Our findings add to a growing evidence base implicating cerebellar involvement in the pathophysiology of PTSD.

A Network-Based Neurobiological Model of PTSD: Evidence From Structural and Functional Neuroimaging Studies.

Although a fine-grained understanding of the neurobiology of posttraumatic stress disorder (PTSD) is yet to be elucidated, the last two decades have seen a rapid growth in the study of PTSD using neuroimaging techniques. The current review summarizes important findings from functional and structural neuroimaging studies of PTSD, by primarily focusing on their relevance towards an emerging network-based neurobiological model of the disorder. PTSD may be characterized by a weakly connected and hypoactive default mode network (DMN) and central executive network (CEN) that are putatively destabilized by an overactive and hyperconnected salience network (SN), which appears to have a low threshold for perceived saliency, and inefficient DMN-CEN modulation. There is considerable evidence for large-scale functional and structural network dysfunction in PTSD. Nevertheless, several limitations and gaps in the literature need to be addressed in future research.

Examining the Crux of Autonomic Dysfunction in Posttraumatic Stress Disorder: Whether Chronic or Situational Distress Underlies Elevated Heart Rate and Attenuated Heart Rate Variability.

Posttraumatic stress disorder (PTSD) has been linked to elevated heart rate (HR) and reduced heart rate variability (HRV) in cross-sectional research. Using ecological momentary assessment and minute-to-minute HRV/HR monitoring, we examined whether cross-sectional associations between PTSD symptom severity and HRV/HR were due to overall elevations in distress levels or to attenuated autonomic regulation during episodes of acute distress. Two hundred nineteen young adults (18-39 years old), 99 with PTSD, underwent 1 day of Holter monitoring and concurrently reported distress levels via ecological momentary assessment. Using multilevel modeling, we examined the associations between momentary distress and the 5-minute means for low-frequency (LF) and high-frequency (HF) HRV and HR immediately following distress ratings, and whether PTSD symptom severity moderated these associations. Compared with the controls, participants with PTSD recorded higher ambulatory distress (mean [standard deviation] = 1.7 [0.5] versus 1.2 [0.3], p < .001) and HR (87.2 [11.8] versus 82.9 [12.6] beats/min, p = .011), and lower ambulatory LF HRV (36.9 [14.7] versus 43.7 [16.9 ms, p = .002) and HF HRV (22.6 [12.3] versus 26.4 [14.6] milliseconds, p = .043). Overall distress level was not predictive of HR or HRV (p values > .27). However, baseline PTSD symptom severity was associated with elevated HR (t(1257) = 2.76, p = .006) and attenuated LF (t(1257) = -3.86, p < .001) and HF (t(1257) = -2.62, p = .009) in response to acute momentary distress. Results suggest that PTSD is associated with heightened arousal after situational distress and could explain prior findings associating PTSD with HR/HRV. Implications for treatment and cardiovascular risk are discussed.

Prospective Memory in Posttraumatic Stress Disorder.

Neuropsychological studies of posttraumatic stress disorder (PTSD) have revealed deficits in attention/working memory, processing speed, executive functioning, and retrospective memory. However, little is known about prospective memory (PM) in PTSD, a clinically relevant aspect of episodic memory that supports the encoding and retrieval of intentions for future actions. Here we examined PM performance in 40 veterans with PTSD compared to 38 trauma comparison (TC) veterans who were exposed to combat but did not develop PTSD. All participants were administered the Memory for Intentions Test (MIST; Raskin, Buckheit, & Sherrod, 2010), a standardized and validated measure of PM, alongside a comprehensive neurocognitive battery, structured diagnostic interviews for psychiatric conditions, and behavioral questionnaires. Veterans with PTSD performed moderately lower than TC on time-based PM, with errors primarily characterized as PM failure errors (i.e., omissions). However, groups did not differ in event-based PM, ongoing task performance, or post-test recognition of PM intentions for each trial. Lower time-based PM performance was specifically related to hyperarousal symptoms of PTSD. Time-based-performance was also associated with neuropsychological measures of retrospective memory and executive functions in the PTSD group. Nevertheless, PTSD was significantly associated with poorer PM above and beyond age and performance in retrospective memory and executive functions. Results provide initial evidence of PM dysfunction in PTSD, especially in strategic monitoring during time-based PM tasks. Findings have potential implications for everyday functioning and health behaviors in persons with PTSD, and deserve replication and future study. (JINS, 2016, 22, 724-734).

Altered Cortico-Limbic Functional Connectivity During an Empathy Task in Subjects with Post-Traumatic Stress Disorder

Empathy is a multidimensional construct consisting of cognitive (inferring mental states) and emotional (empathic concern) components. Emotional empathy is severely impaired in individuals affected by Post-Traumatic Stress Disorder (PTSD). Here, we investigated the neural correlates of such an emotional empathy dysfunction to shed light on the neural circuitry responsible for the social and emotional dysfunction in PTSD. We asked a group of PTSD and a group of healthy controls to solve a Multifaceted Empathy Test, measuring both cognitive and emotional empathy, and investigated the functional connectivity of the cortical areas involved in solving the test. The results revealed that, in healthy individuals, increased neural activity in the frontal cortex modulates activity in the insula while subjects perform the emotional empathy task; whereas, in individuals affected by PTSD, increased activity in limbic regions such the insula and the amygdala modulates activity in the frontal cortex while performing the emotional empathy task. These findings suggest that the lack of cortical top-down control of the frontal cortex on the limbic system in PTSD during empathic processing may explain the emotional and social difficulties experienced by individuals suffering from PTSD.

PTSD and Sexual Dysfunction in Men and Women.

Difficulties in sexual desire and function often occur in persons with posttraumatic stress disorder (PTSD), but many questions remain regarding the mechanisms underlying the occurrence of sexual problems in PTSD. The aim of this review was to present a model of sexual dysfunction in PTSD underpinned by an inability to regulate and redirect the physiological arousal needed for healthy sexual function away from aversive hyperarousal and intrusive memories. A literature review pertaining to PTSD and sexual function was conducted. Evidence for the comorbidity of sexual dysfunction and PTSD is presented, and biological and psychological mechanisms that may underlie this co-occurrence are proposed. This manuscript presents evidence of sexual dysfunction in conjunction with PTSD, and of the neurobiology and neuroendocrinology of PTSD and sexual function. Sexual dysfunction following trauma exposure may be mediated by PTSD-related biological, cognitive, and affective processes. The treatment of PTSD must include attention to sexual dysfunction and vice versa.

Childhood and adult trauma both correlate with dorsal anterior cingulate activation to threat in combat veterans

Prior studies of adult post-traumatic stress disorder (PTSD) suggest abnormal functioning of prefrontal and limbic regions. Cumulative childhood and adult trauma exposures are major risk factors for developing adult PTSD, yet their contribution to neural dysfunction in PTSD remains poorly understood. This study aimed to examine the neural correlates of childhood and adult trauma exposure and post-traumatic stress symptoms (PTSS) within a single model. Method Medication-free male combat veterans (n=28, average age 26.6 years) with a wide range of PTSS were recruited from the community between 2010 and 2011. Subjects completed an emotional face-morphing task while undergoing functional magnetic resonance imaging (fMRI). Clinical ratings included the Clinician-Administered PTSD Scale (CAPS), Childhood Trauma Questionnaire (CTQ) and Combat Exposure Scale (CES). A priori regions were examined through multivariate voxelwise regression in SPM8, using depressive symptoms and IQ as covariates. In the angry condition, CAPS scores correlated positively with activation in the medial prefrontal cortex [mPFC; Brodmann area (BA) 10, z=3.51], hippocampus (z=3.47), insula (z=3.62) and, in earlier blocks, the amygdala. CES and CTQ correlated positively with activation in adjacent areas of the dorsal anterior cingulate cortex (dACC; BA 32, z=3.70 and BA 24, z=3.88 respectively). In the happy condition, CAPS, CTQ and CES were not correlated significantly with activation patterns. dACC activation observed in prior studies of PTSD may be attributable to the cumulative effects of childhood and adult trauma exposure. By contrast, insula, hippocampus and amygdala activation may be specific to PTSS. The specificity of these results to threat stimuli, but not to positive stimuli, is consistent with abnormalities in threat processing associated with PTSS.

Fear conditioning and early life vulnerabilities: two distinct pathways of emotional dysregulation and brain dysfunction in PTSD

The newly proposed criteria for posttraumatic stress disorder (PTSD) in the Diagnostic and StatisticalManual (DSM-V) include dysregulation of a variety of emotional states including fear, anger, guilt, andshame, in addition to dissociation and numbing. Consistent with these revisions, we postulate two models ofemotion dysregulation in PTSD in which fear is not the prevailing emotion but is only one of severalcomponents implicated in a dysregulated emotional system that also mediates problems regulating anger,guilt, shame, dissociation, and numbing.We discuss whether there is a relationship between fear and other emotion regulation systems that may helpfurther our understanding of PTSD and its underlying neurocircuitry. Two pathways describing therelationship between fear and other emotion regulation systems in PTSD are proposed. The first pathwaydescribes emotion dysregulation as an outcome of fear conditioning through stress sensitization and kindling.The second pathway views emotion dysregulation as a distal vulnerability factor and hypothesizes a furtherexacerbation of fear and other emotion regulatory problems, including the development of PTSD afterexposure to one or several traumatic event(s) later in life. Future research and treatment implications arediscussed.

PW01-134 - Limbic and paralimbic cortex grey matter densities are negatively associated with trauma load

ObjectiveThere is converging evidence of gray matter (GM) structural alterations in different limbic structures in Post-Traumatic Stress Disorder (PTSD) patients. The aim of this study was to evaluate GM density in PTSD in relation to trauma load.MethodMagnetic Resonance Imaging (MRI) scans of 21 subjects exposed to occupational trauma, who developed PTSD (S), and of 22 who did not (NS), were performed. The self-rated Trauma Antecedent Questionnaire (TAQ) was administered to assess lifelong trauma load and resilience. TAQ includes two scales (“trauma and neglect” TAQ−, and “resilience factors” TAQ+) further divided into four subscales measuring trauma load and resilience in four different age periods: zero to six, seven to twelve, thirteen to eighteen and adult. Regression analyses between the two sub-scales and GM density were performed on all 43 subjects by means of an optimized Voxel-Based Morphometry (VBM) analysis as implemented in SPM2.ResultsThe analyses showed that GM density negatively correlated only with adult TAQ- in bilateral posterior cingulate, left anterior insula, and right anterior parahippocampal gyrus.ConclusionsIrrespective of the PTSD diagnosis, trauma load was found to correlate with GM density in several limbic structures suggesting a high vulnerability of these structures to the effects of stress and trauma, These regions are implicated in integration, encoding and retrieval of autobiographical and episodic memories, emotional processing, interoceptive awareness and self-referential conscious experience. Thus, our study supports lower GM densities in limbic and paralimbic cortices as a potential structural basis for memory and dissociative dysfunction in PTSD.

Gene Expression Patterns Associated with Posttraumatic Stress Disorder Following Exposure to the World Trade Center Attacks

Although genetic risk factors for posttraumatic stress disorder (PTSD) in similarly traumatized cohorts can be confounded with risk for type of exposure, the primary risk for exposure to the 9/11 attack on New York City was proximity, allowing study of PTSD risk in a sample that is not confounded by exposure-related risk. Thirty-five Caucasians (15 with PTSD, stratified for exposure, age, and gender) were selected from a population-representative sample of persons exposed to the attack from which longitudinal data had been collected in four previous waves. Whole blood gene expression and cortisol levels were obtained. Seventeen probe sets were differentially expressed in PTSD. Identified genes were generally involved in hypothalamic-pituitary-adrenal (HPA) axis, signal transduction, or brain and immune cell function. FKBP5, a modulator of glucocorticoid receptor (GR) sensitivity, showed reduced expression in PTSD, consistent with enhanced GR responsiveness. FKBP5 expression was predicted by cortisol when entered with PTSD severity in regression analysis. Quantitative polymerase chain reaction confirmed significant reductions in FKBP5. Also less expressed in PTSD were STAT5B, a direct inhibitor of GR, and major histocompatibility complex (MHC) Class II. Consistent with observations of HPA axis dysfunction in PTSD, several genes involved in glucocorticoid signaling are differentially expressed among those with current PTSD.

Implications of neuroscientific evidence for the cognitive models of post-traumatic stress disorder

Brewin's dual representation theory, Ehlers and Clark's cognitive appraisal model, and Dalgleish's schematic, propositional, analogue and associative representational systems model are considered in the light of recent evidence on the neural substrates of post-traumatic stress disorder (PTSD). The models' proposals about the cognitive mechanism of memory dysfunction in PTSD are described and evaluated against current knowledge about the neural pathways and functions disrupted in PTSD. A dual pathway model of memory is consistent with neuroscience of memory. The appraisal model also provides an account of the top-down modulation of memory and arousal problems consistent with current neuroscientific evidence of PTSD. Dalgleish's model is less consistent with the evidence because it relies upon assumptions that cannot yet be tested neuroscientifically. All three models under-specify the causal and maintaining influence of hyperarousal relative to the role it plays in current neuroscientific models of PTSD. Implications of the evidence for improving treatment and prevention are discussed.

Cognitive Dysfunctions Associated With PTSD: Evidence from World War II Prisoners of War

The authors aim to delineate cognitive dysfunction associated with posttraumatic stress disorder (PTSD) by evaluating a well-defined cohort of former World War II prisoners of war (POWs) with documented trauma and minimal comorbidities. The authors studied a cross-sectional assessment of neuropsychological performance in former POWs with PTSD, PTSD with other psychiatric comorbidities, and those with no PTSD or psychiatric diagnoses. Participants who developed PTSD had average IQ, while those who did not develop PTSD after similar traumatic experiences had higher IQs than average (approximately 116). Those with PTSD performed significantly less well in tests of selective frontal lobe functions and psychomotor speed. In addition, PTSD patients with co-occurring psychiatric conditions experienced impairment in recognition memory for faces. Higher IQ appears to protect individuals who undergo a traumatic experience from developing long-term PTSD, while cognitive dysfunctions appear to develop with or subsequent to PTSD. These distinctions were supported by the negative and positive correlations of these cognitive dysfunctions with quantitative markers of trauma, respectively. There is a suggestion that some cognitive decrements occur in PTSD patients only when they have comorbid psychiatric diagnoses.

Importance of early environment in the development of post-traumatic stress disorder-like behaviors

A number of clinical studies in which early adversities were defined retrospectively, demonstrated that early adverse experiences increased the morbidity rate of post-traumatic stress disorder (PTSD) in later life. However, no prospective studies have yet been conducted to elucidate whether early adversity affects the risk or severity of PTSD. Thus, we examined whether early adversity would strengthen the severity of PTSD symptoms in later life by using neonatal isolation (NI) and single prolonged stress (SPS) as an animal model of PTSD. We measured anxiety-like behavior in the elevated plus maze (EPM), contextual freezing in the contextual fear (CF) test, and analgesia in the flinch-jump and hot-plate tests in four groups of adult rats (sham, NI, SPS, and NI + SPS). NI significantly enhanced the SPS-induced decrease in the percentage of open arm time and open arm entries in the EPM, enhanced the SPS-induced increase in contextual freezing, and strengthened SPS-induced analgesia, without any changes in locomotor activity in the open field locomotor test. In addition, we examined the effect of environmental enrichment (EE). Repeated exposure to EE ameliorated the NI-induced enhancement of contextual freezing, but not anxiety-like behavior or analgesia, in response to SPS. The results of the present study demonstrated that while early adversity strengthened PTSD-like symptoms, EE alleviated the enhanced contextual freezing by NI and SPS. These findings suggest that early adversity may worsen dysfunction of the amygdala and hippocampus in PTSD, and an early intervention may alleviate the early adversity-mediated enhancement of hippocampal dysfunction in PTSD.

Subtle Neurologic Compromise as a Vulnerability Factor for Combat-Related Posttraumatic Stress Disorder

Previous studies have demonstrated subtle neurologic dysfunction in chronic posttraumatic stress disorder (PTSD) manifest as increased neurologic soft signs (NSSs). The origin of this dysfunction is undetermined. To resolve competing origins of increased NSSs in PTSD, namely, preexisting vulnerability factor vs acquired PTSD sign. Case-control study of identical twins. A Veterans Affairs and academic medical center (ambulatory). A convenience sample of male Vietnam veteran twins with (n = 25) and without (n = 24) PTSD and their combat-unexposed identical (monozygotic) co-twins. Neurologic examination for 45 NSSs. Average scores for 45 NSSs, each scored on an ordinal scale from 0 to 3, masked to diagnosis and combat exposure status. There was a significant between-pair main effect of PTSD diagnosis (as determined in the combat-exposed twin) on average NSS score in the absence of a significant combat exposure main effect or diagnosis x exposure interaction. Combat veterans with PTSD had significantly higher NSS scores than combat veterans without PTSD. The "high-risk," unexposed co-twins of the former also had significantly higher NSS scores than the "low-risk," unexposed co-twins of the latter. This result could not be explained by age, number of potentially traumatic lifetime noncombat events, alcoholism, or the presence of a comorbid affective or anxiety disorder. The average NSS score in unexposed co-twins was not significantly associated with combat severity in combat-exposed twins. These results replicate previous findings of increased NSSs in Vietnam combat veterans with PTSD. Furthermore, results from their combat-unexposed identical co-twins support the conclusion that subtle neurologic dysfunction in PTSD is not acquired along with the trauma or PTSD but rather represents an antecedent familial vulnerability factor for developing chronic PTSD on exposure to a traumatic event.

Impaired P50 sensory gating in post-traumatic stress disorder secondary to urban violence

Previous studies on sensory gating process in post-traumatic stress disorder (PTSD) have yielded conflicting results. To investigate sensory gating function in PTSD we performed a case-control study in a sample of 12 patients with PTSD related to urban violence, compared to 24 normal subjects and 12 schizophrenic subjects evaluating auditory mid-latency evoked potential P50 in a double-click paradigm as a measure of sensory gating. PTSD subjects showed poorer sensory gating as evidenced by higher P50 ratios as compared to normal subjects (85.6% vs. 44.4%, P=0.002). Test and conditioning amplitudes did not differ with statistical significance alone, suggesting a combined effect. Schizophrenic subjects had higher conditioning and marginally smaller test amplitudes when compared to healthy controls, but were not statistically different from PTSD subjects. The present study replicated previous findings of sensory gating dysfunction in PTSD. The pattern of this dysfunction resembles that found in schizophrenia, with both test and conditioning amplitudes possibly implicated. Further studies are still necessary to better understand the pathophysiology of this neurophysiological dysfunction and its nature as a trait or state marker. The P50 paradigm may also become an objective parameter to assess the effects of new treatments for PTSD.

Single-voxel proton MR spectroscopy of right versus left hippocampi in PTSD

Previous magnetic resonance (MR) volume imaging and proton MR spectroscopy studies have suggested a reduction in the hippocampal size and/or neuronal/axonal density in posttraumatic stress disorder (PTSD). The lack of agreement on the laterality of the hippocampal dysfunction prompted this study. A total of 20 veterans (18 men and two women) and one female non-veteran participated in this study conducted in accordance with approved human study protocols. Six of the male veterans and the female non-veteran were without PTSD. Vietnam veterans formed a large subset of the study subjects. Single-voxel proton MR spectra were obtained from the hippocampal region bilaterally on a clinical MR scanner operating at 1.5 T. Analysis of the proton MR spectra showed a decrease in hippocampal NAA/creatine ratio in PTSD subjects significantly higher on the left than the right for the entire study group, as well as for the Vietnam subset. It was concluded that the hippocampal dysfunction in PTSD is lateralized with the left side being more impaired than the right.

Single photon emission computed tomography in posttraumatic stress disorder before and after treatment with a selective serotonin reuptake inhibitor

Background: Posttraumatic stress disorder (PTSD) is recognized as a disorder mediated by specific neurobiological circuits. Functional imaging studies using script-driven trauma imagery and pharmacological challenges have documented altered cerebral function (activation and deactivation) in several brain regions, including the amygdala, hippocampus, prefrontal cortex and anterior cingulate. However, the neural substrates of PTSD remain poorly understood and the effect of selective serotonin reuptake inhibition on regional cerebral activity is deserving of further investigation. Methods: Eleven adult patients (seven men, four women) (mean age+S.D.=33.6±9.2 years) with a DSM-IV diagnosis of PTSD, as determined by the Structured Clinical Interview for DSM-IV (SCID-I) and the Clinician-Administered PTSD Scale (CAPS), underwent single photon emission computed tomography (SPECT) with Tc-99m HMPAO pre- and post-8 weeks of treatment with the selective serotonin reuptake inhibitor, citalopram. Symptoms were assessed at baseline and at 2-week intervals with the Clinician-Administered PTSD Scale (CAPS), Montgomery–Asberg Depression Rating Scale (MADRS), and the Clinical Global Impression Scale (CGI). Image analysis of baseline and post-treatment scans was performed using Statistical Parametric Mapping (SPM). Results: Treatment with citalopram resulted in significant deactivation in the left medial temporal cortex irrespective of clinical response. On covariate analysis, a significant correlation between CAPS score reduction and activation in the left paracingulate region (medial prefrontal cortex) was observed post-treatment. No significant pre-treatment differences were observed between responders and non-responders in anterior cingulate perfusion. Conclusions: These preliminary findings are consistent with clinical data indicating temporal and prefrontal cortical dysfunction in PTSD and preclinical data demonstrating serotonergic innervation of these regions. However, further studies, in particular in vivo receptor imaging studies, are needed to confirm whether these regional abnormalities correlate with clinical features and treatment response.

Event-related potential dysfunction in posttraumatic stress disorder: the role of numbing

The purpose of this study was to examine the relationship between disturbance in event-related potentials (ERPs) and symptom clusters in posttraumatic stress disorder (PTSD). ERPs were recorded in 17 unmedicated civilian PTSD patients and 17 age- and sex-matched controls during a conventional auditory oddball task. PTSD symptom clusters (re-experiencing, active avoidance, numbing, hyperarousal) were correlated with ERP measures. The PTSD group showed ERP disturbances to target stimuli (reduced P200 and P300 and increased N200 amplitude, increased N200 and P300 latency) and reduced P200 amplitude to common stimuli compared to the control group. A significant negative correlation was found between the intensity of numbing symptoms and parietal P300 amplitude. This study replicates findings of disturbed N200 and P300 components in PTSD, reflecting impairments in stimulus discrimination and attention. The finding that numbing was associated with reduced attention processing (P300) is consistent with models positing a relationship between disordered arousal and attention in PTSD.